Effects of quinine on Ca++-induced K+ efflux from human red blood cells.
The Ca++-mediated increase in K+-permeability of intact red blood cells (Gardos effect) was initiated by exposing cells to know concentrations of Ca++ (using EGTA buffers) in the presence of the ionophore A23187. The potency of quinine, an inhibitor of the response, was found to depend on the external K+ concentration. In K+-free solutions the concentration of quinine to achieve 50% inhibition (K50) was 5 microM, but at 5 mM K+ the required concentration was increased 20-fold to 100 microM. An increase in internal Na+ had the opposite effect, allowing a high potency of quinine despite the presence of external K+. Alterations in the internal K+ level, on the other hand, were without effect on the K50, suggesting that the membrane potential is not a factor. This conclusion is supported by the lack of effect on quinine inhibition of substitution of Cl- by NO3-, a considerably more permeant anion. The data are consistent with the hypothesis that quinine inhibits by competitively displacing K+ from an external binding site, the reported K+-activation site for the Ca++-mediated K+-permeability.
D000001:Calcimycin / Q000097:blood; D002118:Calcium / Q000494:pharmacology*; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D066298:In Vitro Techniques; D007700:Kinetics; D011188:Potassium / Q000097:blood*; D011803:Quinine / Q000494:pharmacology*; D012413:Rubidium / Q000097:blood
D000001:Calcimycin; D011803:Quinine; D012413:Rubidium; D011188:Potassium; D002118:Calcium